Saturday, April 23, 2016

Thursday's case, read by 60,000 people, provoked a bit of anguish among readers because they weren't all sure they would recognize this finding of LAD occlusion. Others thought it was obvious. Others thought they would detect it with troponins or serial EKGs (serial EKG was done and did not change; I don't know about serial trops, but one was "negative.") Some persistently denied that the T-wave in V2 was a specific sign of ischemia.

These are 10 cases of LAD occlusion with subtle Hyperacute T-waves in lead V2 (or V3) only.

Steps to verify LAD occlusion, or exclude it:

1. Use of the LAD occlusion/early repolarization formula. But beware the few false negatives, especially when there are hyperacute T-waves but no ST elevation (see Case 2 below):

2. Use contrast echocardiography (This is the most reliable, short of angiography). Bedside echo without contrast or speckle tracking can be misleading. You must be an expert at this to rule out a wall motion abnormality.

Wednesday, April 20, 2016

A 37 year old female with no comorbidities, a non-smoker, with no known hyperlipidemia and no family h/o of CAD presented to ED with central chest pain since 5 hours with no radiation, increased by moving her arms and associated with SOB. This occurred after a stressful interpersonal conflict. She had had similar episodes before when angry or stressed.

"I looked at the ECG and immediately thought "This is an acute LAD occlusion." It is diagnostic of LAD occlusion, but really only to someone who has expertise. You will virtually never see an EKG like this that is a patient's baseline. The T-waves are huge in proportion to the QRS, the QRS amplitude is very small, the T-waves are symmetric and fat, there are sagging ST segments in I, II, V3 and V4. V3 should have some ST elevation, but it actaully has a bit of ST depression."

She was discharged with diclofenac 75 mg IM injection. The pain was relieved.

The patient was discharged home with reassurance and analgesia.

12 hours later the patient was found collapsed at home with no signs of life. The family refused a post-mortem. As she visited our ED within 24 hours from her death, her ECG was reviewed and 50% of the consultants said there is no abnormality of in it. The other 50% said there are hyperacute T waves suggestive of early presentation of MI.

My response:

Sorry to hear about the outcome. This is a very hard ECG for a non-expert to recognize. My hope is that this blog, with cases like this, will educate others about these kinds of subtle findings and prevent future cases like this.

Other comment:

It would have been very helpful to record an ECG after the pain was relieved, to see if there is resolution of the hyperacute T-waves. I would not use absence of change to be reassured that this is NOT ischemia, as it is too abnormal to be anything else. But resolution (change) would be confirmatory evidence.

Learning Points:

1. We all must learn these high risk findings of coronary occlusion.

2. Hyperacute T-waves have a unique morphology. The are like a face that you must recognize.

3. Negative troponins must not be trusted in the setting of an ischemic ECG.I received a good question:So as we move to "rapid rule outs" do you think a second troponin would likely have shown a change? I am trying to understand if this is an acute problem how similar previous episodes are connected vs red herring.My answer:Not necessarily. Even with high sensitivity troponins, there will be false negatives. Not all unstable angina will be detected in the future by hs trop. You will still need to be able to read the ECG. For this patient:1) the artery could spontaneously open up before there is any cell death (i.e., before any elevation of troponin). Then, later, the lesion could close off and kill. Alternatively2) if the artery does not reperfuse, then by the time you have a second troponin back, most of the damage is done.You must be able to recognized these patterns or you will miss an opportunity to make a big difference.

Steve SmithSome more comments and answers that I want to feature:

Comment: Unfortunately without the post-mortem, or more information (which may not have been included in the article for brevity's sake), I would argue it is not possible to say for certain that an MI was missed here. Perhaps the cause of death was overdose, drugs, or some other factor. The fact that the family refused a post-mortem in this situation makes me think something else may have been at play.

Answer: But the EKG is diagnostic of LAD occlusion. That is by far the most likely cause of death.

Comment: T waves are not hyperacute by definition, and it's a difficult scenario. Looking retrospectively it's easy to say an echo would have been helpful but I would have probably done the same except repeating an ecg and two sets of troponins

Answer: They are indeed hyperacute. There is no definition. You just have to learn to recognize it. Denying it will just put you in trouble some day, and that's why I'm trying to teach you. I did not look retrospectively. I saw the ECG before I knew any outcome and knew immediately that it was LAD occlusion. Many of my readers tell me this was obvious, not even subtle. Rather than fighting it, try to learn this morphology. It may save a patient of yours. Learn. Don't be closed-minded.

THANKS to Dr. Stephen Smith for posting this highly illustrative case. There recently has been a good number of similar tracings like this posted on various ECG forums (each with slight variation from the other) — but ALL with virtually the SAME finding — namely that the T waves in lead V2 (and to a lesser extent in lead V3) are disproportionately tall compared to the amplitude of the QRS complex in these leads. And, the responses I’ve seen from even experienced clinicians show the same remarkable range as that reported by Dr. Smith in this Blog — namely that some clinicians correctly recognize the tracing for a DeWinter variant with acute occlusion (or about to be acute occlusion) of the proximal LAD — and others (unfortunately all-too-many other clinicians) call such findings “normal”.

THIS is a tracing that probably should be shown to ALL clinicians (MD and non-MD) who are called upon to analyze acute 12-lead ECGs — both for teaching and perhaps assessment of ECG interpretation ability … In my opinion, this is a case that just should NOT be missed because: i) the patient presented to an ED with 5 hours of chest pain — which should of itself dramatically lower your threshold for what is “normal” vs “abnormal”; ii) the T wave in lead V2 is almost twice QRS amplitude in this lead — and the width of this T wave is comparable to QRS amplitude in this V2 lead. There is no way this is normal in a patient wth new chest pain.

The findings in multiple other leads that Dr. Smith describes are more subtle, but given the picture described by i) and ii), they all support the diagnosis of DeWinter-like T waves.

Dependence on troponins (even the highest of sensitivity troponins) has no place in a case like this. I would be happy initial troponin was negative — since it means that we have recognized this acute LAD occlusion in time to dramatically improve prognosis.

Most cases of anterior hyperacute T waves will not be as glaring as this one is. But attention to the learning points of this case can markedly help to reduce the chance of oversight: i) When a patient presents to the ED with new chest pain — one has to look that much more carefully at their ECG; ii) Engrain the picture of the ST-T wave that we see in lead V3 in your mind. The ST-T wave in V3 is not as obvious as that in V2, but the T wave is still clearly disproportionately taller, fatter at its peak and wider at its base than it should be given QRS amplitude in this lead (Even without V2, this ECG should be of great concern; with V2 this ECG should be alarming); iii) Train your eye to look extra carefully at the “other leads” on the tracing for “patterns”. Virtually every lead on this tracing (except perhaps aVL) has at least a subtle abnormality that taken together in context with the history of new chest pain + obvious abnormality in V2,V3 adds further support of acuity until proven otherwise.

Sunday, April 17, 2016

This was contributed by Dr. Johanna Moore, one of my Hennepin Colleagues who researches CPR, along with Keith Lurie and Demetris Yannopoulos. She translated her research knowledge into a spectacular resuscitation.

Case

A 54 year old male presented via ambulance to the Emergency
Department (ED) in cardiac arrest. He was found down outside a clinic, where
bystander CPR was initiated by clinic staff. The amount of down time was
unclear but thought to be minimal as this was a high traffic pedestrian area.

He received an estimated 5 minutes of manual CPR, then, after medic arrival, 20
minutes of LUCAS CPR, including use of the inspiratory threshold device (ITD, ResQPod) pre-hospital. He was noted to be in refractory ventricular
fibrillation by paramedics. As part of his pre-hospital care, a King airway was
placed, he was defibrillated 7 times, and received 300 mg IV amiodarone, followed by
150 mg IV amiodarone. He also received 2 mg epinephrine. He was noted to be
“chewing” on the King airway and was also given 2 mg IV versed for this.

On arrival to the ED (after 25 minutes of pre-hospital CPR), the patient had agonal respirations
and had brief movements of his upper and lower extremities while on LUCAS. [The
presence of gasping, or agonal, respirations during cardiac arrest is associated
with improved survival1,2.] His continuous end tidal CO2 readings
throughout the case averaged in the 30s mmHg (a sign of effective CPR and good outcome).

LUCAS CPR, with ITD use, was continued. The King airway was exchanged for
an endotracheal tube without interruption of CPR, and blood was noted to be
pooling in the posterior oropharynx at that time. Blood in scant amounts was
also noted to be coming out of the endotracheal tube intermittently. The source
of the blood was unclear.

He was noted to be hypoxic at that time, with initial
recorded oxygen saturation of 70%, and a nadir of 49%. Post intubation, the
oxygen saturation remained low, in the 70-80% range. Several rounds of ACLS medications including
epinephrine, sodium bicarbonate, and calcium gluconate were given along with further defibrillation attempts. The rhythm would intermittently convert to ventricular
tachycardia after defibrillation but would rapidly degenerate into
fibrillation.

Here is an ultrasound of the heart during ventricular fibrillation:

This is fascinating: The septum is fibrillating, but the lateral wall (lower right) is not. As you will see later, this is because the lateral wall is where the STEMI is. It is too ischemic to even fibrillate!

At around 15-20 minutes into the case, the head of the bed
was elevated as much as the LUCAS would allow (10-20 degrees) in an attempt to improve
oxygenation and preserve neurologic function (“Head Up” CPR3,4). The
patient remained in refractory VF. Lidocaine 100 mg IV was given, as well as 2
g of magnesium empirically. 20 mEq KCL was given after the initial potassium
returned at 2.6 mEq/L. The patient remained in refractory VF and an esmolol
bolus, then drip, was started for treatment of ventricular storm.5
Further defibrillation shocks were administered without ROSC. Movement of the
patient during CPR had stopped, but the end tidal CO2 remained over 20 mmHg. His
oxygenation saturation had improved after intubation and placement in the Head
Up position.

Double defibrillation6,7 was then performed by
placing two separate sets of pads on the patient at once, then performing a
simultaneous shock. After 38 minutes of ED CPR and 25 minutes of out of
hospital CPR (total, 63 minutes), ROSC was obtained, with a corresponding increase in end tidal CO2
from the 30 mmHg range to 50 mmHg range. The patient was kept in the Head Up
position. His Chest X-Ray showed diffuse right lung airspace opacities.

Here is a post-ROSC ultrasound:

There is very poor LV function. There is no movement of the lateral wall (lower right). There is also apparent thrombus in the right atrium. With prolonged stasis in cardiac arrest, such thrombi can form. Of course, one must also entertain the possibility of pulmonary embolism as the etiology of the arrest. Ventricular fibrillation is the initial rhythm in less than 5% of arrest from pulmonary embolism.

Here is a parasternal short axis view:

An ECG was obtained:

Sinus rhythm with huge infero-postero-lateral STEMI

The cardiac catheterization lab was activated. Aspirin,
ticagrelor, and heparin were given. Unfortunately, the catheterization lab team
had just started an emergent and complex case, so the cath lab was occupied indefinitely.

Consideration was given to tPA administration for treatment of STEMI, due to the delayed catheterization
time. However, after discussion between the Emergency Physicians and Cardiology
physicians, tPA was not given for the following reasons 1) The patient still
had scant blood coming from the endotracheal tube 2) The consequences of giving
tPA after over 60 min of CPR were unclear and the risk here was thought to be
greater than the benefit 3) The patient would get to cath, albeit not as fast
as the team would like. The ED physicians arranged for the patient to be
transferred to a nearby hospital that had a cardiac catheterization team
available.

The esmolol drip was continued and a low dose epinephrine
drip was started due to hypotension to maintain a MAP greater than 60 mmHg. An
intravascular cooling catheter was placed and therapeutic hypothermia was begun. Transport arrived for the
patient, and he went for catheterization at the outside hospital, which showed
a culprit lesion in the proximal left circumflex artery. A drug eluting stent
was placed.

The patient remains hospitalized at this time, nearly 1
month after his arrest. His hospital course was complicated by an episode of
ventricular tachycardia less than 48 hours post cooling. His post arrest
echocardiogram showed an EF of around 30%, and he had an AICD placed as an
inpatient. At this time, he is being evaluated for vocal cord/speech/swallow
dysfunction, but is otherwise doing well neurologically.

Take Home Points

1.We all already know this, but it is well worth
it to mention again: High quality CPR, with minimal interruption, as well as
bystander CPR, saves lives.

2.There is no absolute way to tell how the brain
is doing during CPR. This is an active area of research among resuscitation
researchers. In this case, good prognostic indicators included the patient
“chewing” on the King airway, agonal respirations noted during CPR,
intermittent movement at the beginning of the ED case during CPR, and end tidal
CO2 readings > 20 mmHg throughout the case.

In spite of these good prognostic signs, many of
the treating ED physicians thought this patient had a very poor chance of neurologic
survival.

3.Head Up position was initiated in the middle of the case and the patient tolerated it well, with no immediate
complications noted. His oxygen saturation level and bloody secretions from the
endotracheal tube also improved in this position.

The animal work performed in
this area uses an angle of 30 degrees for Head Up CPR, which we were not able to achieve. It is also important to remember the theory behind Head Up CPR is not
that it will improve rates of ROSC, but will possibly improve subsequent neurologic
function.

4.Remember esmolol is an option in refractory
ventricular fibrillation, and to use both the bolus and drip dosing.

5.Double defibrillation can also be used in
refractory ventricular fibrillation.

- Use of lidocaine or amiodarone is now proven to increase survival (NNT = 20 for witnessed arrest). Just published in NEJM Apr 13 online.

Friday, April 8, 2016

A late middle-aged man presented with one hour of chest pain. He had significant history of CAD with CABG x5, and repeat CABG x 2 as well as a subsequent PCI of the graft to the RCA (twice) and of the graft to the Diagonal. Most recent echo showed EF of 60%. He also had a history of chronic kidney disease, stage III.

He had recently had a NonSTEMI. Angio had shown some acute disease in the saphenous vein graft to the posterior descending artery off of the RCA. He was managed medically with Clopidogrel. Medics stated that he had not been taking his clopidogrel for 2 weeks.

He appeared to be in shock. Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema.

Here is his ED ECG:

There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI?See below.

The corrected QT interval is extremely long, about 500 ms. This suggests an electrolyte abnormality or a medication effect (acquired long QT). There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Torsades in acquired long QT is much more likely in bradycardia because the QT interval following a long pause is longer still. Thus, Torsades in acquired long QT is called "pause dependent": if there is a sinus beat after a long pause (which creates a longer QT interval), then an early PVC ("early afterdepolarization," EAD) is much more likely to occur during repolarization and to initiate Torsades. The usual sequence is: sinus beat, then early PVC, then a long pause because the PVC was early, which then results in a particularly long QT, then another PVC with "R on T" that initiates torsades.

Here are his medications, none of which prolong the QT:

--Imdur 60mg daily

--Furosemide 40mg BID

--Lisinopril 5mg daily

--Amlodipine 10mg daily

--Digoxin 125mcg q48

--Clopidogrel 75mg daily

--Atorvastatin 20mg daily

--Metoprolol 100mg BID

Clinical Course

His potassium returned at 1.8 mEq/L. This is dangerously low. There is an abundance of literature linking K less than 3.5 to ventricular fibrillation in acute MI (see many references below).

The creatinine was 1.8 mg/dL.

The patient was intubated, given antiplatelet and antithrombotic therapy, 10 mEq of KCl IV was started, and sent to the cath lab.

At cath, he immediately had incessant Torsades de Pointes requiring defibrillation 7 times and requiring placement of a transvenous pacer for overdrive pacing at a rate of 80. He was given amiodarone and lidocaine load and drip and K and Mg drips. After pacing, there was no recurrence of Torsades.

After resuscitation, he was found to have a 90% thrombotic lesion in the same saphenous vein graft to the right posterior descending artery. This was stented.

The patient stabilized.

This subsequent ECG was recorded after the K was up to 2.2 mEq/L:

The STE is resolved.The QT is much shorterThere are now clear U-waves in V2 and V3

2 days later, this ECG was recorded with a K of 3.5:

There is atrial fibrillation. The QT is much shorter still.

The patient stabilized and had a good outcome.

Comments:

STEMI with hypokalemia, especially with a long QT, puts the patient at very high risk of Torsades or Ventricular fibrillation (see many references, with abstracts, below). These two rhythms are often indistinguishable on the monitor or ECG. If there is a pulse, you would call it Torsades. If there is polymorphic VT with a long QT on the baseline ECG, then generally we call that Torsades, but Non-Torsades Polymorphic VT can result from ischemia alone.

However it is classified is not so important! What is important is that the initial treatment is the same for both, especially if there are no pulses: defibrillation, as was done here (NOT synchronized cardioversion).

The fact that it was controlled with overdrive pacing and potassium and magnesium suggests that it was indeed Torsades, but, on the other hand, antidysrhythmics and potassium were also given.

I could find very little literature on the treatment of severe life-threatening hypokalemia. There is particularly little on how to treat when the K is less than 2, and/or in the presence of acute MI. Here are the American Heart Association Guidelines:

"The treatment of hypokalemia consists of minimizing further potassium loss and providing potassium replacement. IV administration of potassium is indicated when arrhythmias are present or hypokalemia is severe (potassium level of less than 2.5 mEq/L). Gradual correction of hypokalemia is preferable to rapid correction unless the patient is clinically unstable.

"Administration of potassium may be empirical in emergent conditions. When indicated, the maximum amount of IV potassium replacement should be 10 to 20 mEq/h with continuous ECG monitoring during infustion A more concentrated solution of potassium may be infused if a central lineis used, but the tip of the catheter used for the infusion should not extend into the right atrium.

"If cardiac arrest from hypokalemia is imminent (i.e., malignant ventricular arrhythmias are present), rapid replacement of potassium is required. Give an initial infusion of 10 mEq IV over 5 minutes; repeat once if needed. Document in the patient's chart that rapid infusion is intentional in response to life-threatening hypokalemia."Comment:
This last section is appropriate for this case. Everyone is appropriately worried about giving K too fast. How much does rapid infustion increase the K? There is, again, little empirical data on this topic that I can find (see 2 studies below, which do not really answer the question). Perhaps there are studies in animals that I have not found?

Total Body Potassium: a 70 kg person has about 7500 mEq of total body K, but the extracellular fluid has only about 48 mEq! Of course the difficulty with K replenishment is that the total body stores may be depleted by far more than can possibly be quickly repleted. The estimated deficit associated with a serum decrease from 4.0 to 3.0 mEq/L is 100-200 mEq of total body K, and from 3.0 to 2.0, the associated loss is double, at 200-400 mEq.* [Sterns RH, et al. Internal potassium balance and
the control of the plasma potassium concentration. Medicine (Baltimore)
1981;60:339-54]. But 100 mEq given all at once would raise the serum K by 30 mEq/L (and be immediately fatal)!!*The NEJM review referenced below (and ACLS, for what that is worth), states that, on average, in a "typical" 70 kg person, the serum K falls by 0.3 mEq/L for every 100 mEq total body deficit. However, this review references the Sterns article above, which by my reading does not state this.Here are some calculations for a safe rapid dose:A 70 kg person has about 5 liters of blood, and 3 liters are serum (2 liters are RBCs). If 10 mEq is given very rapidly, leaving no time for intracellular shift, then it will raise serum K by about 3.3 mEq/L. If the patient is at 1.8, that will raise it to 5.1 mEq/L. One need only get the K above 3.0 to greatly decrease risk (although in STEMI, the optimal level is about 4.0-4.5 mEq/L). 5 mEq rapid bolus would raise this patient's K from by 1.6, from 1.8 to 3.4 mEq/L. The difficulty is in estimating the ongoing shift. As you infuse K, it will start to shift into depleted cells and the serum K will fall again rapidly. Thus, it is critical in patients like this to repeatedly and rapidly, after each bolus, measure the K, and supplement as needed.In the case presented, it is not clear to me that the 10 mEq of K was given rapidly. I suspect it was set to go over 1 hours on a pump, which is the usual practice. It would be difficult to get a nurse to give it faster! However, in this case, it would be appropriate to give it over 5-10 minutes, with monitoring, then immediately measure the K again and be ready to give more.Further complicating the issue is that severe hypokalemia can result in rhabdomyolysis and subsequent K release, with resulting hyperkalemia!Here is review of hypokalemia from the NEJM, but it is mostly about etiology, and says little about rapid replacement in life-threatening hypokalemia EXCEPT to emphasize how dangerous rapid replacement is.Supposedly, patients without ischemia are at low risk of complications from hypokalemia, But it is not entirely without risk. I saw this 30 year old woman with no cardiac disease who was resuscitated from ventricular fibrillation:

Classic Hypokalemia, with large U-waves. K was 1.3 mEq/L.

Learning Points:1. Severe hypokalemia in the setting of STEMI or dysrhythmias is life-threatening and needs very rapid treatment. 5-10 mEq over 5-10 minutes is appropriate for a K of 1.8 mEq/L.2. Be certain that your laboratory value is accurate and that it corresponds with the ECG findings! If the ECG shows no evidence of hypokalemia, it may be an artifactual value. If the ECG shows no evidence, it is unlikely to be life-threatening!3. In a 70 kg person, a 10 mEq bolus will raise serum K by 3.3 mEq/L in the absence of any intracellular shift4. It is optimal to give such a bolus through a central line, but this may not always be possible.5. It is difficult to correct K without also correcting low magnesium. In this case, the Mg was 1.9 mEq/L (within normal limits)6. Learn the management of Polymorphic VT, including Torsades. Literature

Measurements and Results: All patients tolerated the infusions without evidence of hemodynamic compromise, ECG change, or new dysrhythmia requiring treatment. The mean maximum potassium increase was 0.5 +/- 0.3 mmol/L, 0.9 +/- 0.4 mmol/L, and 1.1 +/- 0.4 mmol/L in the 20-, 30-, and 40-mmol groups, respectively. The increase in serum potassium was maximal at the completion of the infusion and was significant (p < .05) compared with baseline in all groups. Peak potassium levels were the same in patients with normal renal function (n = 33) compared with those with renal insufficiency (n = 15).

Urinary excretion of potassium increased in all groups during the infusion and was significant (p < .05) in the 30- and 40-mmol groups, but was no greater in those patients who had received diuretics (n = 8) compared with those patients who had not (n = 40).

Conclusions: In the select group of hypokalemic patients studied, potassium infusions of 20 to 40 mmol delivered over 1 hr were safe to administer and effectively increased serum potassium levels in a dosedependent and predictable fashion. Furthermore, these results were independent of the patient's underlying renal function or associated diuretic administration. (Crit Care Med 1991; 19:694)

Although concentrated infusions of potassium chloride commonly are used to treat hypokalemia in intensive care unit patients, few studies have examined their effects on plasma potassium levels. Forty patients with hypokalemia were given infusions of 20 mmol of potassium chloride in 100 mL of normal saline over 1 hour; 26 patients received the infusions through the central vein and 14 patients through the peripheral vein. Plasma potassium ([K]p) was measured at 15-minute intervals during and after the infusion in 31 patients. ΔK was defined as the difference between each potassium determination and baseline plasma potassium concentration. Continuous electrocardiographic recording was carried out during the infusion and during the 1-hour period immediately preceding the infusion. Mean baseline [K]p was 2.9 mmol/L and all subsequent plasma concentrations significantly increased from baseline. Mean peak [K]p was 3.5 mmol/L, [K]p (1 hour postinfusion) was 3.2 mmol/L, and mean postinfusion ΔK was 0.48 mmol/L (range −0.1–1.7 mmol/L). Arrhythmias, changes in cardiac conduction intervals, and other complications did not occur. The frequency of premature ventricular beats decreased significantly during the infusion compared with that of the control period. The high concentration (200 mmol/L) and rate of delivery (20 mmol/hr) of the potassium chloride infusions were well tolerated, decreased the frequency of ventricular arrhythmias, and did not cause transient hyperkalemia.

Literature on Hypokalemia as a risk for ventricular fibrillation in acute myocardial infarction. All of it comes from the 1980's. Use of diuretics is strongly associated with hypokalemia and ventricular fibrillation in myocardial infarction.

Ten of 59 patients (17%) were receiving a thiazide preparation at the time of an acute myocardial infarction and ventricular fibrillation. Hypokalemia was present in seven of eight patients (87%) receiving thiazides, whereas it was observed in only one of 38 patients (2.6%) not receiving these medications. If hypokalemia is present in patients receiving thiazides who have had an acute myocardial infarction, it should be corrected so as to remove this predisposing cause of ventricular fibrillation.

Over a 13-month period, serum potassium and magnesium levels were measured in 590 patients admitted to a coronary care unit. Hypokalemia, often in the absence of diuretic use, occurred In 17% of the 211 patients with acute myocardial infarction. Patients with acute myocardial infarction and a potassium level of less than 4.0 mEq/L (4.0 mmol/L) had an increased risk of ventricular arrhythmias (59% vs 42%). Because hypokalemia is common in acute myocardial infarction and is associated with ventricular arrhythmias, routine measurement of serum potassium levels and prompt correction are recommended. Hypomagnesemia occurred in only 4% of the patients, but It was more common in the group with acute myocardial infarction than in the group without myocardial infarction (6% vs 3%). Ventricular arrhythmias occurred in ten of the 13 patients with both acute myocardial infarction and hypomagnesemla, but eight of these patients also had low serum potassium levels. This low incidence of hypomagnesemia does not justify routine measurement of serum magnesium levels. However, the mean level (2.5±0.4 mg/dL [1.03 ± 0.16 mmol/L]) in a reference population of healthy volunteers was unexpectedly high and suggests that the low incidence of hypomagnesemia In our population may not be applicable to other centers and may reflect a higher magnesium content in our geographic area of southeastern Ontario.

To evaluate the prevalence of hypokalemia in out-of-hospital cardiac arrest, the initial serum potassium and arterial pH values were reviewed from 138 consecutive patients resuscitated from cardiac arrest. For comparison, the same variables were reviewed for 62 consecutive patients who had transmural acute myocardial infarction (AMI) without cardiac arrest. The mean serum potassium level was lower after resuscitation from cardiac arrest (3.6 ± 0.6 mEq/liter) than during AMI (3.9 ± 0.5 mEq/liter) (p < 0.005). The incidence of hypokalemia (potassium less than 3.5 mEq/liter) was greater in patients sustaining cardiac arrest (41%) than in patients who had AMI without cardiac arrest (11%) (p < 0.001). Hypokalemia was common after cardiac arrest regardless of the occurrence of AMI at the time of arrest. Hypokalemia after cardiac arrest was independent of arterial pH, epinephrine or bicarbonate therapy during resuscitation, or prior therapy with diuretic drugs, digoxin or propranolol. In 10 patients with marked hypokalemia, the serum potassium level returned to normal rapidly (16 hours) during the hospitalization even though only 29% of the predicted potassium requirement was infused before its normalization. Thus, hypokalemia is prevalent immediately after out-of-hospital cardiac arrest, whereas it is uncommon in AMI in the absence of cardiac arrest. The cause and electrophysiologic consequences of this hypokalemia are unknown; in most cases, it is apparently caused by a shift of potassium from the intravascular compartment rather than a total body depletion of potassium.

Sixty patients with a first acute myocardial infarction and no current treatment with cardioactive drugs were included in a prospective study of the relationship between serum potassium concentration and the early occurrence of ventricular tachycardia and premature ventricular contractions (PVCs). Serum potassium level (range 2.5 to 5 mmol/liter) was estimated 3.8 +/- 2.5 hr (mean +/- SD) after the onset of the infarction, and Holter monitoring was performed during the subsequent 12 hr. In multivariate analysis, serum potassium level was negatively and age positively related to ventricular tachycardia. Among the subclasses of PVCs (frequent unifocal, multifocal, couplets, bigeminy), serum potassium concentration was negatively related to the frequent unifocal subclass; hypertension was related to couplets and to the presence of any of the subclasses, and serum aspartate aminotransferase concentration was related to multifocal PVCs. Heart failure leading to death was related to all subclasses of PVC. Serum potassium concentration is an independent inverse predictor of the occurrence of ventricular tachycardia and frequent unifocal PVCs early in acute myocardial infarction.

Serum potassium concentrations obtained on admission to hospital were inversely related to the incidence of ventricular fibrillation in 289 women and 785 men with acute myocardial infarction, 92 of whom developed ventricular fibrillation. Hypokalaemia (serum potassium concentration less than or equal to 3.5 mmol/l) was found in 122 patients (11.4%). The incidence of ventricular fibrillation was significantly greater in patients with hypokalaemia compared with those classified as normokalaemic (serum potassium concentration greater than or equal to 3.6 mmol/l) (17.2% v 7.4%). The increased risk of ventricular fibrillation in the hypokalaemic group was about the same for women and men. While they were in hospital patients with hypokalaemia developed ventricular fibrillation significantly earlier than did normokalaemic patients (median 0.3 hours v 7 hours). Hypokalaemia was more common in women (17.3%) than in men (9.2%), and 55% of the hypokalaemic patients had been treated with diuretics before admission compared with 22% of the normokalaemic group. Hypokalaemia on admission to hospital predicts an increased likelihood and early occurrence of ventricular fibrillation in patients with acute myocardial infarction.

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Disclaimer

Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.